This may be explained by an over-activation of the RAAS, but to further understand the pathophysiology behind the variations in sodium levels in severe COVID-19, prospective studies with structured measurements of serum levels of angiotensin II, aldosterone, AVP, copeptin, urinary sodium, potassium, and osmolality, together with clinical information of fluid and sodium input and output, would be of great value. The gene discussed is AGT; the disease is COVID-19.